Uday Zachariah

How accurate are the Swansea criteria to diagnose acute fatty liver of pregnancy in predicting hepatic microvesicular steatosis

We noted that in two recent reports in Gut , none of 62 patients diagnosed by the Swansea criteria to have acute fatty liver of pregnancy (AFLP) underwent liver biopsy.1 2 We retrospectively assessed the accuracy of the Swansea criteria to predict hepatic microvesicular steatosis in 34 patients with suspected pregnancy-related liver disease who underwent liver biopsy at our centre between 1998 and 2006. These patients tested negative for other causes of acute liver dysfunction such as hepatitis viruses (hepatitis B virus surface antigen (HBsAg), hepatitis C virus (HCV) antibody, immunoglobulin (Ig) M hepatitis A virus (HAV) antibody, IgM hepatitis E virus (HEV) antibody), malarial parasite and sepsis (blood culture). No patient gave a history of ingestion of a potentially hepatotoxic drug. We excluded 10 patients (details in figure 1). Figure 1 Flowchart of patients with suspected pregnancy-related liver disease who underwent liver …

Idiopathic non-cirrhotic intrahepatic portal hypertension: common cause of cryptogenic intrahepatic portal hypertension in a Southern Indian tertiary hospital

Background and aimPatients with intrahepatic portal hypertension and negative etiological work-up for liver disease are often labeled as having cryptogenic cirrhosis. The aim of this study was to evaluate causes of liver disease in patients with unexplained intrahepatic portal hypertension.MethodsWe retrospectively analyzed cause of liver disease in all patients with cryptogenic intrahepatic portal hypertension who underwent liver biopsies between June 2005 to June 2007 in our center.ResultsFive hundred and seventeen patients underwent liver biopsies of whom 227 had portal hypertension. Of these, the cause of liver disease could not be detected prior to liver biopsy in 62 patients. Causes of liver disease identified after liver biopsy in these 62 patients were: idiopathic non-cirrhotic intrahepatic portal hypertension (NCIPH) (30 patients, 48%), cirrhosis (14), fatty liver disease (7) and other causes (11). Initial presentations in idiopathic NCIPH patients were splenomegaly and anemia (18 patients), variceal bleed (9) and ascites (3). Median age (range) of patients at first presentation was 32 (15–57) years, and 19 were male. Majority (90%) were in Child’s class A. Hepatic vein pressure gradient was <5 mmHg in 2 of 7 NCIPH patients tested.ConclusionsWe identified 30 patients with idiopathic NCIPH at our center over the 2 year study period. The clinical presentation and investigations of NCIPH closely mimic cryptogenic cirrhosis. Idiopathic NCIPH should be considered as a differential diagnosis of cryptogenic cirrhosis in India.

Aetiology of paediatric portal hypertension - experience of a tertiary care centre in South India.

The aetiological profile of paediatric portal hypertension in our hospital, a tertiary care centre in South India, showed that the commonest causes were extrahepatic portal venous obstruction (EHPVO) and cirrhosis. Wilsons disease was the most common cause of cirrhosis.

Acute‐on‐chronic liver failure in India: The Indian National Association for Study of the Liver consortium experience

The aim of this study was to analyze etiologies and frequency of hepatic and extrahepatic organ failures (OFs) and outcome of acute‐on‐chronic liver failure (ACLF) at 10 tertiary centers in India.

Acute on chronic liver failure in India: the INASL Consortium experience.

The aim of this study was to analyze etiologies and frequency of hepatic and extrahepatic organ failures (OFs) and outcome of acute‐on‐chronic liver failure (ACLF) at 10 tertiary centers in India.

Non-cirrhotic intrahepatic portal hypertension

This is an introduction to the Gut tutorial “Non-cirrhotic intrahepatic portal hypertension” hosted on BMJ Learning—the best available learning website for medical professionals from the BMJ Group. The diagnosis of non-cirrhotic intrahepatic portal hypertension is often not entertained by doctors due to lack of a clear understanding of this condition. The nomenclature of …

Characterization of hepatitis E virus from sporadic hepatitis cases and sewage samples from Vellore, south India

BACKGROUND Hepatitis E virus (HEV) is endemic in India and causes epidemics and sporadic cases. However, the exact transmission route for sporadic hepatitis E remains unclear. This study investigated HEV in sporadic hepatitis cases and sewage samples, as sewage is the major source of contamination of water in developing countries. METHODS Monthly sampling and testing for HEV in sewage samples from Vellore, India was carried out for 1 year (November 2009-October 2010) and plasma and/or fecal samples from sporadic hepatitis cases presenting to a hospital in Vellore during 2006-2010 were tested for HEV RNA. A total of 144 raw sewage samples and 94 samples from sporadic hepatitis cases were tested for HEV RNA using RT-PCR. RESULTS The prevalence of HEV RNA in sewage and sporadic cases was 55.6% and 9.6%, respectively. HEV strains isolated from sewage showed 94-100% nucleotide sequence similarity with the HEV strains isolated from the sporadic hepatitis cases. HEV RNA in sewage was identified more often during the summer (81.2%) than the monsoon season (14.5%) (p < 0.001). CONCLUSION This study indicates that sewage may be a source of contamination for sporadic hepatitis and also underscores the need for preventive measures to protect drinking water from sewage contamination, particularly in the summer. GENBANK ACCESSION NUMBERS: HEV strains isolated from this study were deposited in GenBank under accession numbers JF972766-JF972773, JN705651-JN705659 and JN705660-JN705662.

Measurement of hepatic venous pressure gradient revisited: Catheter wedge vs balloon wedge techniques

Aims: To evaluate the accuracy of measurement of hepatic venous pressure gradient by catheter wedge as compared to balloon wedge (the gold standard). Materials and Methods: Forty-five patients having a clinical diagnosis of intrahepatic portal hypertension were subjected to the two different types of pressure measurements (catheter wedge and balloon wedge) during transjugular liver biopsy under fluoroscopic guidance. Statistical Analysis: Spearmans rank correlation coefficient, Bland–Altman plot for agreement, and single measure intraclass correlation were used for analysis of data. Results: There was a close correlation between the results obtained by both the techniques, with highly significant concordance (P < 0.0001). Hepatic venous pressure gradients as measured by the catheter wedge technique were either equal to or less than those obtained by the balloon wedge technique. Conclusions: The difference in hepatic venous pressure gradients measured by the two techniques is insignificant.

Budd-Chiari Syndrome Complicating Hydatid Cyst of the Liver Managed by Venoplasty and Stenting

Budd-Chiari syndrome (BCS) and portal hypertension is an uncommon complication of hydatid cyst of the liver. Previous reports describe cyst excision or portosystemic shunt surgery for such patients. Here we present a case of hydatid cyst of the liver with BCS that was treated successfully with hepatic venoplasty and transjugular stent placement.

Rhino-orbital zygomycosis in a patient with pregnancy related liver disease and multi-organ failure

Zygomycosis is an infection due to the fungi Zygomycetes, which, despite being ubiquitous, rarely cause disease in humans. Predisposing conditions include diabetic ketoacidosis, hematologic malignancies, iron overload, multiorgan failure, chronic liver disease, renal failure, metabolic acidosis and immunosuppressed state [1–3]. Zygomycosis can rarely occur in pregnancy as a complication of diabetic ketoacidosis [1]. We report zygomycosis occurring in a non-diabetic woman with pregnancy—related liver disease and multi-organ failure. A 20-year-old woman presented to our center at 38 weeks of gestation (primigravida) with history of swelling of feet and fatigue for 10 days, breathlessness, and jaundice (3 days), and abdominal pain (1 day). She had no prior major illness. She had not taken any drug known to cause liver dysfunction. On presentation, she was conscious and oriented, her blood pressure was 140/90 mmHg, pulse rate was 124/min and respiratory rate was 36/min. She was icteric and pale. Abdominal examination showed a gravid uterus; there was no ascites or palpable mass. Urinalysis revealed proteinuria and pelvic ultrasound showed intrauterine death of the fetus. Her laboratory results were: hemoglobin 13 gm%, white cell count 12,800/cmm, platelet count 56,000/cmm, serum bilirubin 16.6 mg/dL, alanine transaminase 130 IU/L, creatinine 3.4 mg/dL, random blood sugar 160 mg/dL, lactate dehydrogenase 892 IU/L, and INR 4.2. Arterial blood gas analysis showed pH 7.2, lactate 7.3 mmol/L, anion gap 12.6 and, base excess −17.5. Etiological work up for liver dysfunction like peripheral smear for malaria and serology for hepatitis viruses (hepatitis A, B, C and E) was non-contributory. Her blood culture was sterile. A diagnosis of pregnancy—related liver dysfunction [Diagnostic criteria for acute fatty liver of pregnancy (AFLP) and pre-eclamptic liver dysfunction and hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome were met] with intra-uterine death was made. She was started on piperacillin with tazobactam and metronidazole intravenously. After a failed attempt to induce vaginal delivery, she underwent emergency cesarean section under blood product coverage 22 h after admission to our hospital. The baby delivered was a macerated stillbirth. There was 750 mL of ascites drained and 500 mL of blood loss during the surgery. She was maintained on the same antibiotics in intensive care unit and was on mechanical ventilation with other supportive measures. Hemodialysis was instituted, with which acidosis resolved partially (pH 7.35), but she had persistent lactic acidemia (lactate >4 mmol/L) with worsening liver functions and recurrent hypoglycemia. A. Goel (*) :U. Zachariah : C. E. Eapen Department of GI Sciences, Christian Medical College, Vellore 632 004, India e-mail: drashish_goel@yahoo.com